Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Lunatic fringe deficiency cooperates with the Met/Caveolin amplicon to induce basal-like breast cancer

ABSTRACT: Mammary specific deletion of Lfng induces basal-like and claudin-low tumors with accumulation of Notch intracellular domain fragments, increased expression of proliferation-associated Notch targets, amplification of the Met/Caveolin locus, and elevated Met and Igf-1R signaling.

ORGANISM(S): Mus musculus

PROVIDER: GSE35855 | GEO | 2012/05/30

SECONDARY ACCESSION(S): PRJNA151877

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Lunatic fringe deficiency cooperates with the Met/Caveolin amplicon to induce basal-like breast cancer

Project description:Mammary specific deletion of Lfng induces basal-like and claudin-low tumors with accumulation of Notch intracellular domain fragments, increased expression of proliferation-associated Notch targets, amplification of the Met/Caveolin locus, and elevated Met and Igf-1R signaling. Tumor DNAs from Lfngflox/flox; MMTV-Cre conditional mutant mice are being compared to control DNAs from the same animals in order to identify common alterations associated with tumor progression

2012-05-29 | E-GEOD-35855 | biostudies-arrayexpress

Lunatic Fringe Deficiency Cooperates with the Met/Caveolin Gene Amplicon to Induce Basal-Like Breast Cancer

Project description:SUMMARY: Basal breast cancer has been associated with mutations in a number of specific tumor suppressor genes, however, the mechanism by which these tumors express a basal lineage remains unknown. Notch signaling suppresses mammary stem cell (MaSC) self-renewal, while promoting luminal cell fate specification. Here we show that Lfng, a sugar transferase that facilitates Notch activation, suppresses mammary stem/bipotent progenitor cell proliferation. Targeted deletion of Lfng in mammary epithelium induces basal tumors with reduced expression of Notch targets, amplification of the Met/Caveolin gene locus, and elevated Met and Igf-1R signaling. Human basal breast cancer, a disease associated with elevated MET receptor signaling and Caveolin protein, express low levels of LFNG. Thus, reduced LFNG expression cooperates with a Met/ Caveolin amplicon to promote basal breast disease. SIGNIFICANCE: Anti-Notch therapy is currently being tested for efficacy against basal-like breast cancer in humans. Here we report that LFNG, which controls Notch receptor activation, is consistently expressed at a low level in basal tumors and that deletion of this gene in the mouse mammary gland reduces Notch signaling, increases proliferation and induces basal mammary tumors in cooperation with amplification of the Met/Caveolin gene locus. These mutations interact to promote basal gene expression by decreasing Notch pathway activation, as well as to enhance Met and Igf-1R signaling. These pathways can be targeted at multiple levels in humans harboring basal breast cancer with amplification of MET and CAV1/2 32 array samples

2012-05-29 | E-GEOD-28712 | biostudies-arrayexpress

Lunatic Fringe Deficiency Cooperates with the Met/Caveolin Gene Amplicon to Induce Basal-Like Breast Cancer

2012-05-30 | GSE28712 | GEO

Lunatic fringe deficiency cooperates with the Met/Caveolin gene amplicon to induce basal-like breast cancer.

Project description:Basal-like breast cancers (BLBC) express a luminal progenitor gene signature. Notch receptor signaling promotes luminal cell fate specification in the mammary gland, while suppressing stem cell self-renewal. Here we show that deletion of Lfng, a sugar transferase that prevents Notch activation by Jagged ligands, enhances stem/progenitor cell proliferation. Mammary-specific deletion of Lfng induces basal-like and claudin-low tumors with accumulation of Notch intracellular domain fragments, increased expression of proliferation-associated Notch targets, amplification of the Met/Caveolin locus, and elevated Met and Igf-1R signaling. Human BL breast tumors, commonly associated with JAGGED expression, elevated MET signaling, and CAVEOLIN accumulation, express low levels of LFNG. Thus, reduced LFNG expression facilitates JAG/NOTCH luminal progenitor signaling and cooperates with MET/CAVEOLIN basal-type signaling to promote BLBC.

| S-EPMC3603366 | biostudies-literature

Loss of TP53 cooperates with c-MET overexpression to drive hepatocarcinogenesis

Project description:We found that concomitant deletion of Trp53 and overexpression of c-MET (c-MET/sgp53) in the mouse liver led to HCC formation in vivo. Subsequently, a stably passaged cell line derived from a c-MET/sgp53 HCC were generated. We then performed gene expression profiling analysis using data obtained from RNA-seq of the c-MET/sgp53 HCC cell line. Wild-type FVB/N mouse liver were used as control.

2023-07-30 | GSE229764 | GEO

Caveolin-1 Knockout Hearts

Project description:Hearts Lacking Caveolin-1 Develop Hypertrophy with Normal Cardiac Substrate Metabolism Keywords: gene knockout

2009-03-04 | GSE10849 | GEO

Caveolin-3 Knockout Hearts

Project description:Energy Substrate Uptake and Metabolism are Preserved in Hypertrophic Caveolin-3 Knockout Hearts Keywords: gene knockout

2009-03-04 | GSE10848 | GEO

Caveolin-1 knockout liver and gonadal adipose tissue

2012-01-31 | GSE35431 | GEO

Caveolin-1 knockout liver and gonadal adipose tissue

Project description:mRNA expression was compared in between wild type and caveolin-1 knockout livers mRNA expression was compared in between wild type and caveolin-1 knockout gonadal adipose tissue RNA was isolated from livers from male mice in at the light phase RNA was isolated from gonadal adipose tissues from male mice in at the light phase

2012-01-31 | E-GEOD-35431 | biostudies-arrayexpress

Hepatocypte-specific Caveolin-1 knockout livers

Project description:mRNA expression was compared between wild type and hepatocyte-specific caveolin-1 knockout livers in healthy and non-alcoholic fatty liver disease (NAFLD) mice mRNA expression was compared between gender

2020-02-12 | GSE137345 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data